线粒体通透转换孔与心肌缺血-再灌注损伤

缺血-再灌注会导致线粒体通透转换孔（MPTP）的开放,通道的低水平开放和随后的关闭,会导致线粒体释放细胞色素C及其他前凋亡分子,如果开放无限制继续,会导致离子稳态失衡,引起一系列细胞死亡的瀑布式反应。缺血-再灌注期间直接或间接的抑制MPTP开放,对再灌注损伤产生明显的保护作用。近期发现,MPTP短暂的低水平开放对其后的再灌注损伤也有保护作用。作者着重对MPTP的组成及机制、心肌缺血-再灌注时的通透改变和与心肌缺血预处理的关系作一综述,以寻求防治心肌缺血-再灌注损伤的新策略。

Mitochondrial permeability transition pore and myocardial ischemia-reperfusion injury

Ischemia-reperfusion of the heart leads to the opening of mitochondrial permeability transition pore(MPTP).Transient opening and subsequent closure of the MPTP may lead to the release of cytochrome c and other proapoptotic molecules.If unrestrained,this will lead to the loss of ionic homeostasis and initiate the cascade of necrotic cell death.Direct or indirect inhibition of MPTP provides protection against ischemia-reperfusion injury.Recent researches have shown that transient low-conductance pore opening also provides protection against reperfusion injury.This review gives summarization of the components,molecular mechanism of MPTP,permeability transition in myocardial ischemia-reperfusion and the relationship between MPTP and ischemic preconditioning.This may lead to better protective strategies against myocardial ischemia-reperfusion injury in the future.